In the normal human heart, the sinus node, generally located near the junction of the superior vena cava and the right atrium, constitutes the primary natural pacemaker initiating rhythmic electrical excitation of the heart chambers. The cardiac impulse arising from the sinus node is transmitted to the two atrial chambers, causing a depolarization known as a P-wave and the resulting atrial chamber contractions. The excitation pulse is further transmitted to and through the ventricles via the atrioventricular (A-V) node and a ventricular conduction system causing a depolarization known as an R-wave and the resulting ventricular chamber contractions. The normal heart rhythm arising from the sinus node is referred to as a sinus rhythm.
Disruption of the natural pacemaking and conduction system as a result of aging or disease can produce pathologic or non-sinus rhythms. Abnormal heart rhythms can be successfully treated by artificial cardiac pacing using implantable cardiac stimulation devices, including pacemakers and implantable defibrillators, which deliver rhythmic electrical pulses or anti-arrhythmia therapies to the heart at a desired pacing output (amplitude and pulse width) and rate.
A cardiac stimulation device is electrically coupled to the heart by one or more leads possessing one or more electrodes in contact with the heart muscle tissue (myocardium). One or more heart chambers may be electrically stimulated depending on the location and severity of the conduction disorder.
An electrical stimulus delivered to the heart causes the heart to contract when the patient's own intrinsic rhythm fails. To this end, cardiac stimulation devices include sensing circuits that sense the intracardiac electrogram and in particular sense the P-waves and/or R-waves of the intracardiac electrogram.
By monitoring the P-waves and/or R-waves, the sensing circuits of the stimulation device are able to determine the intrinsic rhythm of the heart. When the intrinsic rhythm falters, stimulation pulses can be provided as necessary to induce atrial and/or ventricular depolarizations at appropriate times in the cardiac cycle and thereby maintain a physiologically stable heart rhythm.
Single-chamber, dual-chamber and multi-chamber cardiac stimulation systems now exist. A single-chamber system stimulates and senses in one chamber of the heart (atrium or ventricle). A dual-chamber system stimulates and/or senses in both an atrial chamber and a ventricular chamber of the heart, and multi-chamber systems stimulate and/or sense in three or all four heart chambers.
Dual-chamber systems may be programmed to operate in one of a selection of operating modes. A three letter code (sometimes expanded to a five letter code) is used to describe the basic mode in which the device is operating. The three letter codes refer specifically to electrical stimulation for the treatment of bradycardia (a pathologically slow heart rate). A fourth position (when used) identifies the degree of programmability and rate modulation, and a fifth position (when used) refers to electrical stimulation therapy for the primary treatment of fast heart rhythms or tachycardias.
The first position of the operating code identifies the chamber to which the electrical stimulus is delivered. If the device is not capable of bradycardia support pacing, a “O” occupies this first position. If the device paces in the ventricle, this is indicated by a “V” in the first position; if the device paces in the atrium, this is identified as an “A”. If stimuli can be delivered to both the atrium and the ventricle, the letter “D” is used to reflect dual-chamber stimulation.
The second position of the operating code identifies the chamber or chambers in which sensing occurs. Sensing is the ability of the pacemaker to recognize the intrinsic electrical activity of the heart, e.g., to sense P-waves and/or R-waves. The letters used in the second position are identical to those used in the first position.
The third position of the operating code identifies the way the pacemaker responds to a sensed signal. An “I” means that the stimulation output will be inhibited in response to a sensed intrinsic electrical signal. A “T” in the third position indicates an output stimulus will be triggered in response to a sensed intrinsic electrical signal. A “D” in the third position refers to both response modes.
A popular mode of operation for dual-chamber devices is the DDD mode. DDD systems have been developed to overcome the limitations of previous pacing methods. Specifically, DDD systems provide atrial pacing during atrial bradycardia, ventricular pacing during ventricular bradycardia, and atrial and ventricular pacing during combined atrial and ventricular bradycardia. In addition, DDD systems provide an atrial synchronous mode. Such features more closely approximate the normal response to exercise, or other physiological activity demanding a faster heart rate, by permitting a rate increase to occur commensurate with the rate of the sensed P-wave. This advantageously increases cardiac output and facilitates maintenance of AV synchrony.
In the DDD mode, a signal sensed on the atrial channel will inhibit the atrial output but trigger a ventricular output after a brief delay (the PV delay). If no atrial signal is sensed within a defined atrial escape interval, an atrial stimulation pulse will be delivered and will also trigger a ventricular output after a prescribed AV delay. If a native ventricular depolarization does not occur before the PV or AV delay expires, a ventricular stimulus will be released. If a native ventricular signal is sensed before the PV or AV delay expires, the ventricular output will be inhibited and other timers will be reset. If a native ventricular signal is sensed before the atrial stimulus is released, both the atrial and ventricular output pulses will be inhibited and the various timers will be reset.
The DDD mode possesses the characteristics of truer physiologic pacing because of the advantages in its hemodynamic and electrophysiologic abilities. The DDD mode of operation is designed to mimic the cardiac cycle electronically. Therefore, atrial or ventricular stimulation alone or atrial and ventricular stimulation in sequence will be delivered, so as to continuously maintain atrial and ventricular synchrony over a wide range of rates.
However, the DDD mode of operation can be ineffective in situations in which there is an instable atrial rhythm as evidenced by intermittent atrial flutter/fibrillation or frequent extra-systoles, or slow retrograde atrial activation that triggers ventricular pacing. DDD pacing is ineffective in providing atrial-ventricular synchronous pacing in these situations because the atrium cannot be stimulated, or atrial depolarization cannot be consistently sensed, or the timing of the atrial signal is inappropriate for governing physiological ventricular activation.
Besides these problems associated particularly with the DDD operating mode, there are other general problems with programmable cardiac stimulation devices associated with P-wave detection. Numerous signals may interfere with accurate detection of sinus P-waves. For example, a ventricular stimulation pulse may be sensed by the atrial sensing circuits and mislabeled as a P-wave. Such detection on one channel of the output from another channel is known as “cross talk.”
Ectopic P-waves, which are P-waves arising from a location other than the sinus node, may also be detected and, undistinguished from sinus P-waves, trigger ventricular stimulation. Non-cardiac noise can also interfere with accurate sensing.
R-waves occurring in the ventricles may be of high enough amplitude to be sensed by the atrial sensing circuits. Known as far-field R-waves, these signals may also be misdetected as P-waves. In some patients, a depolarization in the ventricle may, at certain times, be conducted in a retrograde fashion back to the atria causing an atrial depolarization.
Detection of a retrograde depolarization or far-field R-wave as a sinus P-wave will trigger a ventricular stimulation output. If this cycle repeats itself, a pacemaker-mediated tachycardia, a highly undesirable situation, may be induced. Methods for preventing or terminating pacemaker-mediated tachycardia include modulation of the PV delay or the post-ventricular atrial blanking period.
Any of these events detected by the atrial sensing circuits can disrupt the physiological atrial-ventricular synchrony normally provided by DDD pacing or accurate atrial rate detection for the purposes of anti-tachycardia therapy delivery. Patients susceptible to atrial fibrillation may also be submitted to dynamic atrial overdrive pacing in which the atrium is paced at a rate higher than the intrinsic rate. This overdrive pacing acts to suppress the onset of atrial fibrillation. Inaccurate rate detection due to sensing of non-sinus events, however, could cause the atrium to be paced at a higher rate than necessary during dynamic atrial overdrive pacing. Therefore, various blanking schemes have been introduced that prevent detection of unwanted cross talk, far-field signals or retrograde P-waves. A post ventricular atrial blanking period (PVAB) is a period of absolute blanking of the atrial sensing circuit during the delivery of a ventricular stimulation pulse to prevent cross talk. A post-ventricular atrial refractory period (PVARP) is a relative refractory period during which signals may be sensed by the atrial sensing circuits but are generally presumed to be a far-field R-wave or a retrograde P-wave and are thus ignored and not used for tracking.
The disadvantage of using such blanking and refractory periods is that high atrial rates may go undetected when sinus P-waves do occur during a blanking or refractory interval. It is therefore desirable to accurately detect high atrial rates in order to provide appropriate corrective action. Known methods for responding to a high atrial rate include anti-tachycardia pacing and automatic device operating mode switching. By changing the operating mode from DDD to a single chamber mode, for example VVI, the high atrial rate is no longer tracked by the ventricular output.
It is desirable, therefore, to detect sinus P-waves and distinguish these signals from noise, ectopic P-waves (also known as premature atrial contractions), retrograde P-waves, or far-field R-waves. By accurately detecting and distinguishing sinus and non-sinus events sensed by the atrial sensing circuits, the stimulation device may respond appropriately in terms of ventricular tracking of the atrial rate, avoiding pacemaker-mediated tachycardia, delivering anti-tachycardia therapies, and executing atrial suppression algorithms.
In the ventricular channel, cross talk sensing occurs when the ventricular sensing circuits sense an atrial stimulation pulse. The atrial stimulation pulse is incorrectly detected as an intrinsic R-wave. The likelihood of cross talk occurring is increased when the programmed ventricular sensitivity is high or the atrial stimulation pulse amplitude is high. The undesirable consequence of cross talk sensing is the inhibition of a ventricular stimulation pulse when in fact ventricular pacing is needed.
One solution to cross talk sensing is the application of a ventricular blanking period, which is an absolute blanking period following an atrial stimulation pulse, combined with a “Ventricular Safety Standby” feature (VSS). This Ventricular Safety Standby (VSS) feature prevents inappropriate inhibition of the ventricular output when cross talk signal detection occurs. When Ventricular Safety Standby is enabled, a cross talk detection window begins immediately after the ventricular blanking interval terminates. The cross talk detection interval is set to a specified value minus the ventricular blanking interval. If the ventricular channel senses an event during the cross talk detection window, the event is presumed to be cross talk, and a ventricular stimulation pulse is delivered at a specified interval after the atrial pulse. If the AV interval is programmed to a value less than the specified value, the ventricular pulse is delivered at the end of the interval. Additionally, if a ventricular event is sensed after the cross talk window terminates, then the pending ventricular pulse is inhibited. While this feature ensures that the ventricle will be stimulated in situations of cross talk, discrimination between actual cross talk and true ventricular activity is not made.
For tracking pacing modes (such as DDD or DDT), not distinguishing between the presence of intrinsic ventricular activity and cross talk could lead to the delivery of a stimulation pulse during a T-wave, which can induce ventricular tachycardia in susceptible patients. By combining morphology discrimination with a method to characterize cross talk, the stimulation device can determine whether a sensed ventricular event is cross talk or a true intrinsic event and respond in the safest manner possible.
Thus, it is desirable, in a cardiac stimulation device, particularly in dual chamber or multichamber cardiac stimulation devices, to provide methods for clearly discriminating between cardiac sinus events and any other events that may be sensed including non-sinus events, cross talk, or far-field events. It is further desirable to provide a uniquely prescribed response to each of these identified events to ensure appropriate device function and the greatest level of safety for the patient.